Exercise in obese female rats has beneficial effects on maternal and male and female offspring metabolism

• Published in: International Journal of Obesity 2015-04, Vol.39 (4), p.712-719
• Main Authors: Vega, C C, Reyes-Castro, L A, Bautista, C J, Larrea, F, Nathanielsz, P W, Zambrano, E
• Format: Article
• Language: English
• Subjects: 631/443/319; 692/699/2743/393; 692/700/459; Adiposity; Animal Nutritional Physiological Phenomena; Animals; Bioenergetics; Blood Glucose - metabolism; Body composition; Body fat; Breastfeeding & lactation; Cholesterol; Corticosterone; Diabetes; Diet; Diet, High-Fat; Economic conditions; Energy metabolism; Epidemiology; Exercise; Exercise therapy; Female; Females; Fertility; Glucocorticoids; Glucose; Health aspects; Health Promotion and Disease Prevention; Insulin; Insulin Resistance - physiology; Internal Medicine; Intervention; Laboratory animals; Lactation; Lactation - metabolism; Leptin; Leptin - blood; Male; Maternal Nutritional Physiological Phenomena; Maternal-fetal exchange; Medicine; Medicine & Public Health; Metabolic Diseases; Metabolism; Obesity; Obesity - metabolism; Offspring; original-article; Oxidative stress; Patient outcomes; Physical Conditioning, Animal; Physiological aspects; Pregnancy; Pregnancy, Animal; Prenatal Exposure Delayed Effects - metabolism; Public Health; Rats; Rats, Wistar; Sex differences; Socioeconomics; Triglycerides; Weaning; Weight; Womens health
• ISSN: 0307-0565; 1476-5497
• DOI: 10.1038/ijo.2013.150

Background: Maternal obesity (MO) impairs maternal and offspring health. Mechanisms and interventions to prevent adverse maternal and offspring outcomes need to be determined. Human studies are confounded by socio-economic status providing the rationale for controlled animal data on effects of maternal exercise (MEx) intervention on maternal (F0) and offspring (F1) outcomes in MO. Hypothesis: MO produces metabolic and endocrine dysfunction, increases maternal and offspring glucocorticoid exposure, oxidative stress and adverse offspring outcomes by postnatal day (PND) 36. MEx in part prevents these outcomes. Methods: F0 female rats ate either control or obesogenic diet from weaning through lactation. Half of each group wheel ran (from day 90 of life through pregnancy beginning day 120) providing four groups ( n =8/group)—(i) controls, (ii) obese, (iii) exercised controls and (iv) exercised obese. After weaning, PND 21, F1 offspring ate a control diet. Metabolic parameters of F0 prepregnancy and end of lactation and F1 offspring at PND 36 were analyzed. Results: Exercise did not change maternal weight. Before breeding, MO elevated F0 glucose, insulin, triglycerides, cholesterol, leptin, fat and oxidative stress. Exercise completely prevented the triglyceride rise and partially increases glucose, insulin, cholesterol and oxidative stress. MO decreased fertility, recovered by exercise. At the end of lactation, exercise returned all metabolic variables except leptin to control levels. Exercise partially prevented MO elevated corticosterone. F1 offspring weights were similar at birth. At PND 36, MO increased F1 male but not female offspring leptin, triglycerides and fat mass. In controls, exercise reduced male and female offspring glucose, prevented the offspring leptin increase and partially the triglyceride rise. Conclusions: MEx before and during pregnancy has beneficial effects on the maternal and offspring metabolism and endocrine function occurring with no weight change in mothers and offspring indicating the importance of body composition rather than weight in evaluations of metabolic status.